On the Pathophysiology of Stroke‐Associated Pneumonia: A Brief Review

ABSTRACT Stroke is often accompanied by fatal complications, such as stroke‐associated pneumonia (SAP). In order to protect the injured brain from further damage while preventing SAP, it is important to understand the pathophysiology of SAP. This review aims at the pathophysiology of SAP, including poststroke innate and adaptive immune responses, sterile inflammation, and the bidirectional communication along the gut–brain and gut–lung axis. The response to brain injury is characterized by innate and adaptive immune processes activated over the whole body. In the acute stage of stroke, damage‐associated molecular patterns released from injured parenchyma trigger pro‐inflammatory intracellular signaling to recruit immune cells to infiltrate the ischemic parenchyma. In the chronic stage, the adaptive immunity is critical to maintain homeostatic in limiting the degree of inflammation. Such immunodepression is not limited to the brain and may lend the patient to the risk of SAP. The communications between gut and brain via the gut–brain axis may be essential to maintain homeostatic in the poststroke stage. Elucidating the intricate interplay between the immune system and the injured brain is essential for understanding the pathophysiology of SAP.